Location: Animal Diseases Research
Title: Fibroblasts express OvHV-2 capsid protein in vasculitis lesions of American bison (Bison bison) with experimental sheep-associated malignant catarrhal fever Authors
|Nelson, Danielle -|
|Davis, William -|
|Brown, Wendy -|
|O'Toole, Donal -|
|Oaks, Lindsay -|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 16, 2013
Publication Date: October 25, 2013
Citation: Nelson, D.D., Taus, N.S., Schneider, D.A., Cunha, C.W., Davis, W.C., Brown, W.C., Li, H., O'Toole, D., Oaks, L.J. 2013. Fibroblasts express OvHV-2 capsid protein in vasculitis lesions of American bison (Bison bison) with experimental sheep-associated malignant catarrhal fever. Veterinary Microbiology. j.vetmic.2013.07.021. Interpretive Summary: Sheep-associated malignant catarrhal fever (SA-MCF) caused by ovine herpesvirus-2 (OvHV-2) is an often fatal disease of American bison. How OvHV-2 causes disease in bison is not completely understood. In this study we examined tissues of bison with experimentally induced SA-MCF using a recently developed antibody against the major structural protein of OvHV-2. Co-labeling with cellular markers showed that activated fibroblasts were the specific cell type expressing the viral structural protein. This is the first in vivo identification of fibroblasts infected with a gammaherpesvirus. More studies are needed to determine the role of infected fibroblasts in the development of SA-MCF in bison.
Technical Abstract: Sheep-associated malignant catarrhal fever (SA-MCF) caused by ovine herpesvirus-2 (OvHV-2), a '-herpesvirus, is an often fatal disease characterized by lymphoproliferation, vasculitis, and mucosal ulceration in American bison (Bison bison), cattle (Bos taurus), and other clinically susceptible species. The pathogenesis and cellular tropism of OvHV-2 infection in bison has not been fully defined. Transcripts of open reading frame 25 (ORF25) encoding the viral capsid protein have been detected in peripheral blood leukocytes and tissues of bison with SA-MCF. Since there is evidence of OvHV-2 DNA within lymphocytes but not within vascular structural cells, we hypothesized that perivascular lymphocytes express ORF25 protein within vascular lesions of bison. This hypothesis was refuted by the demonstration of ORF25 protein in activated fibroblasts but not lymphocytes within the vascular tunica adventitia in six bison with experimentally-induced SA-MCF. These findings provide a novel foundation for defining the pathogenesis of vasculitis in bison with SA-MCF.